Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0172)
Name
Allicin
Synonyms
Allicin; 539-86-6; Diallyl thiosulfinate; S-allyl prop-2-ene-1-sulfinothioate; Diallyldisulfid-S-oxid; Thio-2-propene-1-sulfinic acid S-allyl ester; Allylthiosulphinic acid allyl ester; DADSO; S-Allyl acrylo-1-sulphinothioate; 2-Propene-1-sulfinothioic acid, S-2-propenyl ester; C6H10OS2; CCRIS 9053; S-allyl 2-propene-1-sulfinothioate; EINECS 208-727-7; UNII-3C39BY17Y6; BRN 1752823; 3-prop-2-enylsulfinylsulfanylprop-1-ene; 2-Propene-1-sulfinothioic acid S-2-propenyl ester; CHEBI:28411; 3C39BY17Y6; 2-Propene-1-sulfinic acid, thio-, S-allyl ester; CHEMBL359965; DTXSID6043707; 3-[(prop-2-ene-1-sulfinyl)sulfanyl]prop-1-ene; 4-04-00-00007 (Beilstein Handbook Reference); S-prop-2-en-1-yl prop-2-ene-1-sulfinothioate; S-2-PROPEN-1-YL 2-PROPENE-1-SULFINOTHIOATE; allimin; diallyl disulfide-oxide; allylthiosulfinate; Allicin kit; 3-allylsulfinylsulfanylprop-1-ene; Allicin, tech. grade; Diallyldisulfid-S-oxide; Allicin (not validated); Dianyctrsnlgide;Allisatin; ALLICIN [MI]; ALLICIN [WHO-DD]; ALLICIN(TECH GRADE); SCHEMBL2920; GTPL2419; 2-Propene-1-sulfinothioic Acid S-2-Propen-1-yl Ester; DTXCID4023707; JDLKFOPOAOFWQN-UHFFFAOYSA-N; 3-allylsulfinylsulfanyl-prop-1-ene; BCP08391; HY-N0315; BDBM50240948; MFCD00468100; NSC707388; s3860; AKOS006282482; ALLICIN (CONSTITUENT OF GARLIC); CCG-266298; DB11780; FD10435; NSC-707388; 3-(prop-2-enylsulfinylthio)-1-propene; AC-34150; XA162045; XA176305; CS-0008813; FT-0621982; ALLICIN (CONSTITUENT OF GARLIC) [DSC]; C07600; EN300-217463; S-2-Propenyl 2-propene-1-sulfinothioate, 9CI; A829889; Q409641; Q-200609; 2-Propene-1-sulfinothioic acid, S-2-propenyl ester (9CI); Diallyl thiosulfinate and Allylthiosulphinic acid allyl ester; Diallyldisulfid-S-oxid, 3-prop-2-enylsulfinylsulfanylprop-1-ene

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Status
Investigative
Drug Type
Small molecular drug
Structure
Formula
C6H10OS2
IUPAC Name
3-prop-2-enylsulfinylsulfanylprop-1-ene
Canonical SMILES
C=CCSS(=O)CC=C
InChI
InChI=1S/C6H10OS2/c1-3-5-8-9(7)6-4-2/h3-4H,1-2,5-6H2
InChIKey
JDLKFOPOAOFWQN-UHFFFAOYSA-N
PubChem CID
65036
TTD Drug ID
D0X9YD
Full List of Ferroptosis Target Related to This Drug
Unspecific Target
In total 3 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Oesophageal cancer ICD-11: 2B70
 Disease Info 
Responsed Regulator Ubiquitin-like modifier-activating enzyme ATG7 (ATG7) Driver
 Regulator Info 
Pathway Response mTOR signaling pathway hsa04150
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE-510 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1354
HET-1A cells Normal Homo sapiens CVCL_3702
In Vivo Model
All mice were housed in a specific pathogen-free environment under a standard 12 h light-dark cycle at 25 and had ad libitum access to food and water. Approximately 4 x 106 KYSE510 cells in 100 uL of normal saline were subcutaneously injected into the right flank of mice (n = 20 in total). All mice were allocated to a control or 10 mg/kg allicin group (n = 10 per group), as previously described (Suddek 2014). The mice were orally administered allicin or normal saline once daily for 28 days.

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Response regulation In summary, allicin may induce cell death in esophageal squamous cell carcinoma (ESCC) cells by activating AMPK/mTOR-mediated autophagy and ferroptosis. Furthermore, ATG5 and ATG7 expression increased in tumors after allicin treatment. In contrast, NCOA4 expression increased, but the protein level of FTH1 and TfR1 decreased in tumors after allicin treatment.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Oesophageal cancer ICD-11: 2B70
 Disease Info 
Responsed Regulator Serine/threonine-protein kinase mTOR (MTOR) Suppressor
 Regulator Info 
Pathway Response mTOR signaling pathway hsa04150
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE-510 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1354
HET-1A cells Normal Homo sapiens CVCL_3702
In Vivo Model
All mice were housed in a specific pathogen-free environment under a standard 12 h light-dark cycle at 25 and had ad libitum access to food and water. Approximately 4 x 106 KYSE510 cells in 100 uL of normal saline were subcutaneously injected into the right flank of mice (n = 20 in total). All mice were allocated to a control or 10 mg/kg allicin group (n = 10 per group), as previously described (Suddek 2014). The mice were orally administered allicin or normal saline once daily for 28 days.

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Response regulation In summary, allicin may induce cell death in esophageal squamous cell carcinoma (ESCC) cells by activating AMPK/mTOR-mediated autophagy and ferroptosis. Furthermore, ATG5 and ATG7 expression increased in tumors after allicin treatment. In contrast, NCOA4 expression increased, but the protein level of FTH1 and TfR1 decreased in tumors after allicin treatment.
Experiment 3 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Responsed Disease Oesophageal cancer ICD-11: 2B70
 Disease Info 
Responsed Regulator Autophagy protein 5 (ATG5) Driver
 Regulator Info 
Pathway Response mTOR signaling pathway hsa04150
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE-510 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1354
HET-1A cells Normal Homo sapiens CVCL_3702
In Vivo Model
All mice were housed in a specific pathogen-free environment under a standard 12 h light-dark cycle at 25 and had ad libitum access to food and water. Approximately 4 x 106 KYSE510 cells in 100 uL of normal saline were subcutaneously injected into the right flank of mice (n = 20 in total). All mice were allocated to a control or 10 mg/kg allicin group (n = 10 per group), as previously described (Suddek 2014). The mice were orally administered allicin or normal saline once daily for 28 days.

    Click to Show/Hide
Response regulation In summary, allicin may induce cell death in esophageal squamous cell carcinoma (ESCC) cells by activating AMPK/mTOR-mediated autophagy and ferroptosis. Furthermore, ATG5 and ATG7 expression increased in tumors after allicin treatment. In contrast, NCOA4 expression increased, but the protein level of FTH1 and TfR1 decreased in tumors after allicin treatment.
Nuclear receptor coactivator 4 (NCOA4)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Oesophageal cancer ICD-11: 2B70
 Disease Info 
Pathway Response mTOR signaling pathway hsa04150
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model TE-1 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1759
KYSE-510 cells Esophageal squamous cell carcinoma Homo sapiens CVCL_1354
HET-1A cells Normal Homo sapiens CVCL_3702
In Vivo Model
All mice were housed in a specific pathogen-free environment under a standard 12 h light-dark cycle at 25 and had ad libitum access to food and water. Approximately 4 x 106 KYSE510 cells in 100 uL of normal saline were subcutaneously injected into the right flank of mice (n = 20 in total). All mice were allocated to a control or 10 mg/kg allicin group (n = 10 per group), as previously described (Suddek 2014). The mice were orally administered allicin or normal saline once daily for 28 days.

    Click to Show/Hide
Response regulation In summary, allicin may induce cell death in esophageal squamous cell carcinoma (ESCC) cells by activating AMPK/mTOR-mediated autophagy and ferroptosis. Furthermore, ATG5 and ATG7 expression increased in tumors after allicin treatment. In contrast, NCOA4 expression increased, but the protein level of FTH1 and TfR1 decreased in tumors after allicin treatment.
References
Ref 1 Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling. Heliyon. 2022 Oct 12;8(10):e11005. doi: 10.1016/j.heliyon.2022.e11005. eCollection 2022 Oct.